MicroRNA‐520g induces epithelial–mesenchymal transition and promotes metastasis of hepatocellular carcinoma by targeting SMAD7. Issue 1 (29th November 2014)

• Record Type: Journal Article
• Authors: Kan, Heping; Guo, Wenbin; Huang, Yuqi; Liu, Dingli
• Is Part Of: FEBS letters. Volume 589:Issue 1(2015)
• Page Start: 102
• Page End: 109
• Publication Date: 2014-11-29
• Subjects: HCC -- hepatocellular carcinoma -- EMT -- epithelial–mesenchymal transition -- SMAD7 -- SMAD family member 7 -- ER -- estrogen receptor -- PR -- progesterone receptor -- MicroRNA-520g -- Hepatocellular carcinoma -- Epithelial–mesenchymal transition -- SMAD family member 7 -- Cancer metastasis; Biochemistry -- Periodicals; Biophysics -- Periodicals; Molecular biology -- Periodicals; Biochimie -- Périodiques; Biochemistry; Biophysics; Molecular biology; Periodicals; 572.05
• DOI: 10.1016/j.febslet.2014.11.031
• Languages: English
• ISSNs: 0014-5793

Abstract

Abstract : Hepatocellular carcinoma (HCC) is the third leading cause of cancer‐related death worldwide. Aberrant expression of miRNAs contributes to HCC development. Here, we observed elevated miR‐520g expression in tumor samples from HCC patients with relapse and metastasis, and this high miR‐520g expression was correlated with poor survival. Through gain‐ and loss‐of‐function studies, miR‐520g was demonstrated to facilitate HCC cell migration, invasion and epithelial–mesenchymal transition (EMT). SMAD7 was identified as a direct target of miR‐520g. Accordingly, we conclude that high miR‐520g expression promotes HCC cell mobility and EMT by targeting SMAD7, and this is correlated with reduced survival in HCC patients. Abstract : MiR‐520g is obviously up‐regulated in HCC tissues and cells. High miR‐520g expression correlates with poor prognostic features and short survival. Up‐regulation of miR‐520g promotes HCC cell migration, invasion and EMT. SMAD7 is a direct target of miR‐520g. SMAD7 functions in elevated miR‐520g‐induced HCC cell mobility and EMT.